tetano
Editor, Senior Moderator
Am J Case Rep
. 2025 Apr 28:26:e947416.
doi: 10.12659/AJCR.947416. Post-COVID-19 Guillain-Barré Syndrome with GM1 and GD1b Antibodies: A Case Study and Literature Review
Mrudula Thiriveedi[SUP] 1 [/SUP], Francis G Sto Domingo[SUP] 2 [/SUP], Sawyer Longley[SUP] 2 [/SUP], Siddharth Patel[SUP] 1 [/SUP], Sujatha Baddam[SUP] 3 [/SUP], Anil Chimakurthy[SUP] 4 [/SUP]
Affiliations
BACKGROUND The coronavirus disease 2019 (COVID-19) pandemic, caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has led to the emergence of various neurological complications, including Guillain-Barre syndrome (GBS). GBS is an acute, immune-mediated disorder characterized by progressive weakness, sensory deficits, and autonomic dysfunction. Anti-ganglioside antibodies are often seen in GBS; however, they are rarely reported in the setting of COVID-19-related GBS. We present a case of post-COVID-19 GBS with positive GM1 and GD1b antibodies. CASE REPORT An 86-year-old man presented with progressive quadriparesis, sensory deficits, and hyporeflexia 4 weeks after COVID-19 infection. Brain and spine imaging were unremarkable. Cerebrospinal fluid (CSF) analysis revealed albuminocytological dissociation, consistent with acute inflammatory demyelinating polyneuropathy (AIDP). Despite 2 courses of intravenous immunoglobulin (IVIG), the patient showed minimal improvement in muscle strength. Nerve conduction studies (NCS) revealed severe sensorimotor polyneuropathy, with axonal and demyelinating features. Serum testing showed elevated GM1 and GD1b anti-ganglioside antibody titers. CONCLUSIONS Although numerous cases of COVID-19-related GBS have been reported, anti-ganglioside antibody positivity, particularly GM1 and GD1b, is uncommon. The underlying mechanism is presumed to be autoimmune, likely triggered by molecular mimicry. Our case contributes to the evolving understanding of GBS immunology in the context of COVID-19. Although this case report may not alter current GBS management, the co-occurrence of GM1 and GD1b antibodies in post-COVID-19 GBS underscores the need for continued vigilance, immunological profiling, and research into potential prognostic and therapeutic implications.
. 2025 Apr 28:26:e947416.
doi: 10.12659/AJCR.947416. Post-COVID-19 Guillain-Barré Syndrome with GM1 and GD1b Antibodies: A Case Study and Literature Review
Mrudula Thiriveedi[SUP] 1 [/SUP], Francis G Sto Domingo[SUP] 2 [/SUP], Sawyer Longley[SUP] 2 [/SUP], Siddharth Patel[SUP] 1 [/SUP], Sujatha Baddam[SUP] 3 [/SUP], Anil Chimakurthy[SUP] 4 [/SUP]
Affiliations
- PMID: 40293968
- DOI: 10.12659/AJCR.947416
BACKGROUND The coronavirus disease 2019 (COVID-19) pandemic, caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has led to the emergence of various neurological complications, including Guillain-Barre syndrome (GBS). GBS is an acute, immune-mediated disorder characterized by progressive weakness, sensory deficits, and autonomic dysfunction. Anti-ganglioside antibodies are often seen in GBS; however, they are rarely reported in the setting of COVID-19-related GBS. We present a case of post-COVID-19 GBS with positive GM1 and GD1b antibodies. CASE REPORT An 86-year-old man presented with progressive quadriparesis, sensory deficits, and hyporeflexia 4 weeks after COVID-19 infection. Brain and spine imaging were unremarkable. Cerebrospinal fluid (CSF) analysis revealed albuminocytological dissociation, consistent with acute inflammatory demyelinating polyneuropathy (AIDP). Despite 2 courses of intravenous immunoglobulin (IVIG), the patient showed minimal improvement in muscle strength. Nerve conduction studies (NCS) revealed severe sensorimotor polyneuropathy, with axonal and demyelinating features. Serum testing showed elevated GM1 and GD1b anti-ganglioside antibody titers. CONCLUSIONS Although numerous cases of COVID-19-related GBS have been reported, anti-ganglioside antibody positivity, particularly GM1 and GD1b, is uncommon. The underlying mechanism is presumed to be autoimmune, likely triggered by molecular mimicry. Our case contributes to the evolving understanding of GBS immunology in the context of COVID-19. Although this case report may not alter current GBS management, the co-occurrence of GM1 and GD1b antibodies in post-COVID-19 GBS underscores the need for continued vigilance, immunological profiling, and research into potential prognostic and therapeutic implications.